|List |< first << previous [record 2 of 2]|
|Mutation Type||Other Transgenic|
|Strain of Origin|
|Alleles Listed at MGI|
JAX strain name: B6.Cg-Ndor1Tg(UBC-cre/ERT2)1Ejb/2J
Stock No: 008085
Mice hemizygous for this Cre-ERT2 transgene are viable and fertile. Mice from this founder line have strong tamoxifen-inducible cre activity in all reported tissue types. The Cre-ERT2 fusion protein consists of Cre recombinase fused to a triple mutant form of the human estrogen receptor; which does not bind its natural ligand (17β-estradiol) at physiological concentrations but will bind the synthetic estrogen receptor ligands 4-hydroxytamoxifen (OHT) and, with lesser sensitivity, ICI 182780. Restricted to the cytoplasm, Cre-ERT2 can only gain access to the nuclear compartment after exposure to OHT. To counteract the mixed estrogen agonist effects of tamoxifen injections, which can result in late fetal abortions in pregnant mice, progesterone may be coadministered. When these Cre-ERT2 mice are bred with mice containing a loxP-flanked sequence of interest, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the flanked sequences in widespread cells/tissues.
|Nature of Mutation||
These transgenic mice express a Cre-ERT2 fusion gene under the control of the human ubiquitin C (UBC) promoter.
When these Cre-ERT2 mice are bred with mice containing a loxP-flanked sequence of interest, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the flanked sequences in widespread cells/tissues.
NOTES: This assay will NOT distinguish hemizygous from homozygous transgenic animals.
Transgene = ~475 bp
Ruzankina Y; Pinzon-Guzman C; Asare A; Ong T; Pontano L; Cotsarelis G; Zediak VP; Velez M; Bhandoola A; Brown EJ. 2007. Deletion of the developmentally essential gene ATR in adult mice leads to age-related phenotypes and stem cell loss. Cell Stem Cell 1(1):113-26 PubMed: 18371340